Neuropathology of Cognitively Normal Elderly
By D. Knopman, Joseph E. Parisi, A. Salviati, M. Floriach-Robert, Brad Boeve, R. Ivnik, Glenn E. Smith, D. Dickson, Keith A. Johnson, Lindsay E. Petersen and 3 more. Journal of Neuropathology and Experimental Neurology, 2003
676 citations recorded by the source corpus.
Subfields: Neurology, Physiology, Psychiatry and Mental health
View Paper: https://www.semanticscholar.org/paper/535bb8fbe023fef3805d828bc58dcdca3cc2ebf9
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Neurology
- Dennis W. Dickson
- D. Selkoe
- John Q. Trojanowski
- D. Thal
- Thomas Wisniewski
- J. Attems
- E. Masliah
- H. Braak
In Physiology
- Dennis W. Dickson
- D. Selkoe
- Clifford R. Jack Jr.
- Bradley T. Hyman
- John Q. Trojanowski
- E. Masliah
- Reisa A. Sperling
- Thomas Wisniewski
In Psychiatry and Mental health
- Dennis W. Dickson
- Clifford R. Jack Jr.
- Ronald C. Petersen
- John Q. Trojanowski
- William J. Jagust
- Thomas Wisniewski
- David S. Knopman
- K. Jellinger
Citations in the corpus
- Comparison of multiple tau-PET measures as biomarkers in aging and Alzheimer's disease (2017, methodology): “Consistent with neuropathological data, more than 40% of MCI patients included in our study were categorized as Braak ROIbased stage III/IV (Knopman et al., 2003).”
- Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological cascade (2010, neutral): “…AD is a hypothesis rather than a statement of fact, because some of these individuals will die without ever expressing clinical symptoms.3– 5 The hypothetical assumption is that an asymptomatic individual with pathological changes that are indicative of AD would ultimately have become…”
- Defining imaging biomarker cut points for brain aging and Alzheimer's disease (2017, neutral): “Similarly, around 30% of clinically normal elderly individuals have AD at autopsy [21] or have biomarker evidence of amyloidosis [22– 24], and therefore, a clinically defined “unaffected” non-AD control group also has significant inherent error [17].”
- Deciphering the molecular basis of memory failure in Alzheimer's disease. (2004, background): “Importantly, are detected in a significant proportion of the nondein a rare case of the translocation form of Down's synmented elderly (Knopman et al., 2003).”
- The overlap between vascular disease and Alzheimer’s disease - lessons from pathology (2014, background): “, small or large cerebral infarcts, lacunes, and WMLs, in up to 10% [10,165-167].”
- Religious Orders Study and Rush Memory and Aging Project (2018, neutral): “These data complement data from other clinical-pathologic stud-iesillustratingthatADpathologyispresentinpersonswithoutdementia[351–353].”
- Neuropathological alterations in Alzheimer disease. (2011, background): “Longitudinal prospective clinicopathological studies in nondemented elderly people have revealed that up to 45% of nondemented elderly would meet the NIA-RI criteria for AD had they been demented, usually the intermediate likelihood category of these criteria, and rarely the high likelihood category”